PediatricEducation.org™http://pediatriceducation.org
A Pediatric Digital Library and Learning Collaboratory intended to serve as a source of continuing pediatric education, curated by Donna M. D'Alessandro M.D. and Michael P. D'Alessandro M.D.Tue, 03 Mar 2015 22:35:47 +0000enhourly1http://wordpress.com/http://s2.wp.com/i/buttonw-com.pngPediatricEducation.org™http://pediatriceducation.org
What Causes Vesicular Exanthams?http://pediatriceducation.org/2015/03/02/what-causes-vesicular-exanthams/
http://pediatriceducation.org/2015/03/02/what-causes-vesicular-exanthams/#commentsMon, 02 Mar 2015 00:19:39 +0000http://pediatriceducation.org/?p=2638Continue reading →]]>Patient Presentation A 3-year-old male came to clinic with a history of fever and developing rash for 24 hours. The fever had been 38.2°C maximum and was responsive to antipyretics. The rash had been noticed during the night and was described as small spots on his arms and trunk. Since then they had developed a central vesicle. All the lesions looked the same, and the mother didn’t think that more were appearing. The family denied any travel. There were sick children at daycare but the family didn’t know what specific problems were occurring. There was no cough, emesis, diarrhea, pain or pruritus. He had rhinorrhea and had been drinking well but was refusing most solids. He was not particularly fatigued, lethargic or irritable. The past medical history showed a healthy child who was fully immunized. The review of systems was otherwise negative.

The pertinent physical exam showed a well-appearing child with a temperature of 38.3°C. Heart rate was 106 beats/minute and respiratory rate was 24/minute. HEENT showed no mucosal involvement, no oral lesions and his tympanic membranes were normal. He had mild clear rhinorrhea. Heart, lungs and abdominal examinations were negative. His skin had ~ 20 lesions that were distinct lesions, scattered on the upper torso and upper arms. They were 4-10 mm in size with a red, blanching base. Most had a central vesicle that was 2-3 mm in size with water-like fluid. All the lesions looked the same. There were no excoriations seen. There were no lesions on the palms or soles.

The diagnosis of a vesicular exanthem was made that was most likely due to a viral etiology such as coxsackie disease. He had a relative who had frequent contact with him and who was immunocompromised. Therefore a lesion was unroofed and a swab was sent for varicella polymerase chain reaction. The patient was started on acyclovir for possible varicella but when the test returned negative the acyclovir was stopped. When the physician contacted the mother the next day, she reported that the lesions had not progressed, his fever was lower and he was drinking well.

DiscussionVesicles are circumscribed, elevated, fluid-filled lesions < 1 cm on the skin. They contain serious exudates or a mixture of blood and serum. They last for a short time and either break spontaneously or evolve into bullae. They can be discrete (e.g. varicella or rickettsial disease), grouped (e.g. herpes), linear (e.g. rhus dermatitis) or irregular (e.g. coxsackie) in distribution.

Associated symptoms such as pruritus, fever, myalgias, coryza and cough, along with a history of potential contact can be helpful. Vesicular rashes that are associated with systemic findings such as fever are usually due to infectious diseases (especially viruses and bacteria), while those that do not have systemic findings often are due to contact or infectious diseases that are non-respiratory contacts such as scabies or tinea.

Most patients do not need specific testing as the clinical history and physical examination will often be enough. In certain cases, scraping of the lesion to look for parasites (i.e. scabies) or multinucleated giant cells (i.e. herpes) or fungus may be indicated.

Most treatment is supportive. Topical agents such as calamine lotion or oatmeal baths may provide some relief. Medication for pain and pruritus can be helpful. Treatment for specific diseases such as acyclovir for herpes, antibiotics for bacterial disease and antifungal mediation for fungal diseases should be recommended as appropriate.

Bullae are also fluid-filled epidermal lesions that are filled with serous or seropurulent fluid. They are > 1 cm and often easily rupture due to their thin walls. The differential diagnosis is different for bullae than for vesicular lesions and is often more ominous including such diseases as Steven-Johnson, staphylococcal scalded skin and meningococcemia.

Vesicular or bullous exanthems should be investigated more extensively if there is skin sloughing, petechiae or purpura, fever and irritability, inflammation of the mucosa, urticaria, has respiratory distress, and diarrhea or abdominal pain.

Learning Point
The differential diagnosis for vesicular exanthems includes:

Viral

Coxsackie

Echo

Herpes

Smallpox

Varicella

Bacteria

Haemophilus

Staphylococcus

Streptococcus

Mycoplasma

Fungal

Trichophyton mentagrophytes

Tricophyton rubrum

Parasitic

Rickettsial diseases

Scabies

Tularemia

Other

Contact and Rhus dermatitis

Dishidrotic eczema

Kawasaki disease

Photosensitivity

Questions for Further Discussion
1. What is the differential diagnosis of bullous exanthems?
2. What is the difference between a pustular lesion and those that are vesicular or bullous?

http://pediatriceducation.org/2015/03/02/what-causes-vesicular-exanthams/feed/0pediatriceducationminHow Do You Diagnose Hypermobility?http://pediatriceducation.org/2015/02/23/how-do-you-diagnose-hypermobility/
http://pediatriceducation.org/2015/02/23/how-do-you-diagnose-hypermobility/#commentsMon, 23 Feb 2015 00:18:35 +0000http://pediatriceducation.org/?p=2636Continue reading →]]>Patient Presentation A 16-year-old female came to clinic with a history of knee pain for 5 months. She had twisted the right knee during cheerleading practice and despite appropriate rest, exercise and strength building that was overseen by the school trainers, she still was having intermittent knee pain. The pain occurred off and on in both knees, not necessarily concurrently. It seemed worse after a heavier workout. She had pain also intermittently at night that would occasionally awaken her. She denied any swelling, erythema, difficulty walking, stiffness, weight loss, fever, skin or vision changes. Her past medical history was significant for multiple musculoskeletal pain episodes that occurred with exercise. Her mother said, “She always seems to be doing something to herself and is more clumsy. When she is running she easily trips over things.” The social history showed she was an avid cheerleader, dancer and runner. The family history was positive for rheumatoid arthritis and joint hypermobility.

The pertinent physical exam revealed a well-appearing female in no distress, normal vital signs and growth parameters in the 50% (weight) and 95% (height). Eye examination showed no obvious lens abnormalities. Cardiac examination had a regular rate and rhythm without a murmur. Abdomen was negative. Skin had no discolorations, apparent thinness, or stretch marks. Musculoskeletal examination showed no erythema or edema of any joint. She had full range of motion in all her joints and no specific pain could be elicited. She was able to oppose her thumbs to her forearm, hyperextend her 5th fingers, and could place her hands flat on the ground with forward trunk flexion. It was not clear if she could hyperextend her knees or elbows.

The diagnosis of probable generalized joint hypermobility was made. The pediatrician discussed this with the family as well as other possibilities including rheumatological diseases (later blood testing was normal). Because of the risk of Marfan syndrome, an echocardiogram was ordered (later also normal) while the patient was awaiting a genetics consultation appointment for possible Marfan syndrome or Ehlers-Danlos syndrome. The patient was also referred to orthopaedics and physical therapy for education and ongoing management of her current and probable future musculoskeletal problems.

DiscussionHypermobility can be seen in several different clinical entities. These include generalized joint hypermobility, joint hypermobility syndrome, Marfan syndrome, Ehlers-Danlos syndrome and Osteogenesis Imperfecta. For adults, a Beighton score of at least 4 or 5 is used as a definition of hypermobility. For children a score of 5 or 6 is used as a definition. (see scoring system below).

Generalized joint hypermobility is hypermobility with few or no symptoms. If they occur, knee symptoms are the most common.

Joint hypermobility syndrome has hypermobility along with other symptoms such as pain, reduced muscle strength, and decreased proprioception and balance.

Joint hypermobility syndrome is diagnosed by:

2 major criteria

1 major criteria and 2 minor criteria

4 minor criteria

2 minor criteria and a close relative who has been diagnosed with JHS

Major Brighton criteria

Beighton score of four or more – either now or in the past

Joint pain for > 3 months in 4 or more joints

Minor criteria

Beighton score of 1-3, or having a Beighton score of 0-3 if age > 50 years

Joint pain > three months up to three joints, back pain for longer than three months, or spondylosis or spondylolisthesis

Dislocation or partial dislocation of > one joint, or the same joint more than once

> 3 soft tissue injuries – i.e. bursitis, tenosynovitis

Marfanoid habitus

Abnormal skin

Eye symptoms – i.e. ptosis, hyperopia

Varicose veins, hernia, or uterine prolapse

Learning PointBeighton tests are clinical maneuvers that are dichotomously scored. A total score from 0-9 is calculated with a higher score being associated with hypermobility.
They have been shown to have high inter-rater reproducibility for adults and children.

Beighton scores
Items 1-4 are scored 1 point for each side, item 5 has 1 point only. Add total points for score

http://pediatriceducation.org/2015/02/23/how-do-you-diagnose-hypermobility/feed/0pediatriceducationminHow Common is Gout?http://pediatriceducation.org/2015/02/16/how-common-is-gout/
http://pediatriceducation.org/2015/02/16/how-common-is-gout/#commentsMon, 16 Feb 2015 00:16:46 +0000http://pediatriceducation.org/?p=2634Continue reading →]]>Patient Presentation A 12-year-old female came to clinic with a 3 month history of ankle pain. It initially started in the right ankle after she had turned her ankle during dancing. This got somewhat better but then her left ankle and foot also became more painful. She had continued her activities which included multiple dance activities, gymnastics, Tae Kwon Do and two weeks previously she had started cross-country running. The pain had increased in the couple of days after she started cross-country. The running occurred mainly on sidewalks and roads. She said she had no pain in the morning but it slowly increased over the day and was worse when she started her activities in the afternoon or evening. Sometime she would limp during practices. The pain decreased with rest after the activities and with warm baths. She denied any pain at night, swelling or warmth of the joint, night sweats, weight loss, rashes, fevers or chills. She denied any other joints being affected. The past medical history was non-contributory. The family history had no specific orthopaedic, rheumatologic or immune problems. The pertinent physical exam revealed a healthy female with growth parameters in the 10-50%. She was tall and thin. The ankles, feet and toes did not show any erythema or edema. No specific pain could be elicited. The joints were freely mobile. The rest of her extremities, back, and TMJ joints were negative. She had no skin changes.

The radiologic evaluation showed no bony changes in the feet or ankles. The diagnosis of general overuse resulting in ankle pain was made. The patient was instructed to significantly decrease or stop her activities and let her body rest more until the pain subsided. She then could increase her activities as tolerated. She had a health maintenance examination already scheduled in 3 weeks so followup would be done then. After the visit the medical student was reviewing the differential diagnosis of joint pain with the attending and included gout as one of the entities. “I’ve only seen hyperuricemia with patients with tumor lysis syndrome or with a metabolic problem. I’ve never seen gout. It’s really an adult disease and certainly on the differential diagnosis for adults, but we really don’t see it in children,” the attending noted.

Discussion
Purines are heterocyclic aromatic organic compounds. Common ones are adenine, guanine, xanthine, hypoxanthine, uric acid and caffeine. The most common sources of purines are meat (especially liver, kidney, and brain), certain fish (herring, mackerel, anchovies, sardines), and in lower amounts in beans, and certain plants and yeast. Purines are synthesized, used by the body, then they are degraded by a variety of enzymes. They then can be salvaged to resynthesize purines or are eliminated primarily by the kidney.

When intake or synthesis outweighs elimination then hyperuricemia can result. Hyperuricemia can occur in patients with obesity and metabolic syndrome, psoriasis, medications (thiazide diuretics), genetic diseases such as Lesch Nyhan disease, and kidney disease including transplantation. Myeloproliferative disease including leukemia, lymphoma and tumor lysis syndrome also have increased risk of hyperuricemia.

Hyperuricemia can lead to the deposition of monosodium urate crystals in the joint and periarticular tissue. Crystal deposition stimulates interleukin-1 release from monocytes that causes an inflammatory response. Painful joints and gout are the result. Overtime gouty trophi may occur that can cause bony erosions. As it can take 20 years or more for this process of hyperuricemia and crystal deposition to occur, gout generally does not occur often in the typical pediatric patient. Therefore gout is not usually considered in the differential diagnosis of joint or limb pain in the pediatric population as it is in the adult population.

Learning Point
In the adult population, gout had a prevalence rate of 1.4 – 4% in the western countries of the United States, United Kingdom, Germany and Australia.Juvenile gouty arthritis is uncommon in the pediatric population. A review found only 66 cases of primary gout over a period from 1769-1971.

Secondary gout occurs more often but is uncommon too occurring in the diseases listed above. In adult renal transplant patients hyperuricemia (80%) and gout (10%) are frequent complications. In the pediatric renal transplant populations, one study found 50% of patients had hyperuricemia, but rarely had gout. The gout occurred > 5 years after transplant.

Questions for Further Discussion
1. What is the differential diagnosis of joint swelling?
2. What signs and symptoms are consistent with idiopathic juvenile arthritis?
3. What is pseudogout?

http://pediatriceducation.org/2015/02/16/how-common-is-gout/feed/0pediatriceducationminHow Do You Treat Water for Cryptosporidium?http://pediatriceducation.org/2015/02/09/how-do-you-treat-water-for-cryptosporidium/
http://pediatriceducation.org/2015/02/09/how-do-you-treat-water-for-cryptosporidium/#commentsMon, 09 Feb 2015 00:24:01 +0000http://pediatriceducation.org/?p=2622Continue reading →]]>Patient Presentation A 16-year-old male came to clinic with several days of diarrhea that he describes as loose and watery and occurred with some urgency. He denied blood in the stool, fevers, chills, nausea, emesis, abdominal cramping or rashes. He denied any significant weight loss and was urinating well. He had been camping with several other teenage boys just before the diarrhea occurred. They had camped on farmland that was used for dairy animals and crops. “We drank the water from the creek but we did boil it,” he said. He said at least one other camper also had diarrhea. The past medical history showed a healthy male with several athletically-related orthopaedics injuries.

The pertinent physical exam showed a well-developed male. His weight was the same as at a recent well-child examination. His abdominal examination was negative. The diagnosis of a diarrheal illness caused by viral, bacterial or protozoan organisms was made. As he was otherwise well and was well-hydrated, no specific treatment was done but continued hydration and good hygiene was advised. The laboratory evaluation of stool cultures for bacteria and parasites were sent because of the illness duration. The state epidemiology laboratory did extended testing because of the history and diagnosed Cryptosporidium. The state epidemiology team followed up with the patient and the contacts but all had improved when contacted.

DiscussionCryptosporidium is an oocyte-forming coccidian protozoan. It is transmitted through ingestion of contaminated food, water, or contact with infected persons or animals (particularly preweaned calves). It is a common cause of diarrhea from contaminated recreational water supplies including lakes, ponds, streams, and pool and waterpark water. It has been associated with occupational exposures in agricultural settings and veterinary schools. Emergencies where calves or biological samples are involved have caused transmission of Cryptosporium to first responders. Others at risk include young children and those who care for them (i.e. parents, child care professionals), swimmers who swallow contaminated water, those exposed to human feces through sexual contact, and domestic and international travelers. Travelers who drink unfiltered, untreated water are at higher risk. People who are immunocompromised are also at higher risk.

The most common symptom is watery diarrhea that begins about 7-10 days (range 2-26 days) after infection and is self-limited. Excretion can be intermittent and last for weeks. Other symptoms are abdominal cramps, decreased appetite and weight loss, emesis, fever, fatigue, headache and joint pain. Cryptosporidium testing is usually not included in routine ova and parasite testing so specific testing often needs to be requested. Multiple stool samples may be needed because of the intermittent excretion.

Immunocompetent patients are usually not treated, but nitazoxanide can be used for both immunocompetent and immunocompromised patients.

Learning Point
Recreational water supplies are a common source as the pool chemicals (often halogens such as chlorine and bromine) are ineffective against Cryptosporidium. Even well maintained facilities can have tainted water and small amounts can cause disease. Cryptosporium can lives for days outside the host. It is a very hearty organism and difficult to kill.

Bathers should not use recreational water if they have open cuts, or sores to help prevent transmission. Swallowing water is never recommended. Inadequately treated water should be avoided. This includes ice or water from lakes, streams, ponds, rivers, springs or shallow wells where the water may be unsafe. Water supplies can be appropriately treated for Cryptosporidum by:

Using bottled water instead including for personal hygiene and food preparation.

Heating the water to a rolling boil and boiling for 1 minute.

Using a water filter. This should be with an absolute pore size of 1 micrometer or smaller or use of an NSF Standard 53 or NSF Standard 58 filter for cyst and oocyst reduction. If a filter is used, then the water will still need additional treatment to kill or inactivate viruses and bacteria.

Using chlorine dioxide (not the pool chemical) appropriately

Using ultraviolet light appropriately

Detailed information regarding water disinfection for travelers can be found here.

Questions for Further Discussion
1. List other infectious diseases transmitted primarily through water.
2. What are the common causes of traveler’s diarrhea and how is it treated?

http://pediatriceducation.org/2015/02/09/how-do-you-treat-water-for-cryptosporidium/feed/0pediatriceducationminHow Good is 5-Fluorouracil to Treat Plantar Warts?http://pediatriceducation.org/2015/02/02/how-good-is-5-fluorouracil-to-treat-plantar-warts/
http://pediatriceducation.org/2015/02/02/how-good-is-5-fluorouracil-to-treat-plantar-warts/#commentsMon, 02 Feb 2015 00:28:09 +0000http://pediatriceducation.org/?p=2625Continue reading →]]>Patient Presentation A 4-year-old male came to clinic for treatment of plantar warts that had been present for less than a month. His mother had tried salicylic acid inconsistently and wanted cryotherapy. The past medical history showed a healthy male and the review of systems was normal.

The pertinent physical exam a healthy male with normal vital signs and growth parameters. On the ball of the left foot and great toe he had two flat, but cauliflower-like lesions of ~3-4 mm in size that were relatively superficial. The diagnosis of plantar warts was made. The resident was reviewing his treatment plan with his attending and said that he was going to write a prescription for “WartPEEL®” as one of his other attendings liked that medication instead of plain salicylic acid. His current supervisor asked him what was in the medication and a website showed that it was 5-Fluorouracil and salicylic acid in a proprietary formula. The attending asked the resident about if there was any data that 5FU was more efficacious than plain salicylic acid and what was the difference in cost. The resident wasn’t sure so he said he would try to look into this over the next few days.

DiscussionVeruccae plantaris or plantar warts are caused by Human papillomavirus which causes benign epidermal tumors that often have a cauliflower pattern on the foot that may be elevated or flush with the surrounding skin. Lesions may resemble calluses but the normal footprint pattern is disrupted. The lesions often have pinpoint hemorrhages that appear as black dots. In an immunocompetent individual, the lesions usually have spontaneous resolution within 2 years but the infection may spread to create additional lesions. The lesions may also cause pain or discomfort because of their size or location.

Plantar warts are often difficult to treat. Treatments include keratolytics (e.g. salicylic acid (SA) or tricholoacetamic acid), cryotherapy with liquid nitrogen, electrodesiccation, or direct surgical removal. Suffocation by duct tape and plastic have also been used. Immunotherapy with candida, mumps or trichophytin antigens have been used more recently. These are felt to induce a local and distant immunoresponse that destroys the lesions.

5-Fluorouracil (5FU) is an antineoplastic and antimetabolite that inhibits DNA and RNA synthesis which is believed to be the mechanism that stops wart proliferation WartPEEL®. WartPEEL® is a compounded medication available only in certain locations in the United States.

Learning Point Warts are difficult to treat. It takes a long time to treat them. Relapse and spread are common. There can be pain and discomfort with each treatment or with no treatment also. Cost and often daily treatments makes the treatment often difficult to comply with.

Placebo cure rates for wart treatment are around 20-40% for many trials and trials often have end points between 3-6 months.

http://pediatriceducation.org/2015/02/02/how-good-is-5-fluorouracil-to-treat-plantar-warts/feed/0pediatriceducationminWhat is the Remission Rate for Antithyroid Drug Treatment for Hyperthyroidism in Children?http://pediatriceducation.org/2015/01/26/what-is-the-remission-rate-for-antithyroid-drug-treatment-for-hyperthyroidism-in-children/
http://pediatriceducation.org/2015/01/26/what-is-the-remission-rate-for-antithyroid-drug-treatment-for-hyperthyroidism-in-children/#commentsMon, 26 Jan 2015 00:01:37 +0000http://pediatriceducation.org/?p=2610Continue reading →]]>Patient Presentation A 12-year-old female came to clinic for her health maintenance examination. She had no complaints and her mother had no concerns until her daughter was weighed and there was a slower increase in her weight over the year. The patient had normal eating and activity and they denied weight loss. She was sleeping well without night sweats, had normal elimination and was doing well in school. She had a history of being a more anxious child but this was unchanged. The family also denied any skin or hair changes. The past medical history was negative except for some normal acute illnesses. The family history was positive for diabetes, stroke and arthritis. The review of systems was otherwise normal.

The pertinent physical exam showed a well-appearing Asian female with a heart rate of 108 beats/minute, blood pressure of 106/56, respiratory rate of 20 and she was afebrile. Her height was 90% and tracking normally. Her weight had always been at the 95% and was now at the 90%. HEENT revealed very subtle proptosis with the eyelids still covering part of the irises. Her thyroid was diffusely enlarged without palpable nodes and there was no murmur over the organ. She had some shoddy anterior cervical adenopathy. Heart was mildly tachycardic without a murmur. She had normal skin without hair loss or increased perspiration. Neurological examination found a mild tremor of her hands when they were outstretched and she seemed somewhat anxious to the examiner. She also had mild hyperreflexia in all extremities. The laboratory evaluation showed a thyroid stimulating hormone of < 0.1 microU/mL (normal 0.5-4.7 microU/mL), and a free T4 of 3.9 ng/dL (normal 0.8-2.7 ng/dL).

The diagnosis of hyperthyroidism with thyrotoxicosis was made and pediatric endocrinology was consulted by telephone. An appointment for evaluation was made for 2 days later. The radiologic evaluation of a thyroid ultrasound found a mildly diffusely enlarged organ without nodules. Additional laboratory testing was positive for TSH receptor antibodies consistent with Grave’s disease. She began treatment with the antithyroid drug methimazole.

Discussion

The thyroid gland secrets two hormones – T4 which is a prohormone and T3 which is the biologically active hormone. Receptors for T3 are found in nearly all body tissues. T3 regulates metabolism and energy production. Organs most affected are the heart, liver and central nervous system as well as growth of the fetus and child. Hyperthyroidism is common with a prevalence rate of about 1-2% for women and 0.2% for men. The most common cause of thyrotoxicosis is Grave’s disease where autoantibodies to thyroid stimulating hormone (TSH) exist. These autoantibodies attach to thyroid tissue TSH receptors and increase the production of T4 and T3. Grave’s disease often co-occurs with other autoimmune diseases such as diabetes, Hashimoto’s thyroiditis, rheumatoid arthritis and also with Turner’s, Down’s and Di George syndromes. Children only account for about 1-2% of all patients with Grave’s disease.

Antithyroid drugs (ATD) – The most common drugs used are carbimazole and its active metabolite methimazole (MMI) and propylthiouracil. Propylthiouracil is usually not used because of the risk of severe hepatitis.
MMI is the most common first line drug used and is taken orally daily. Side effects include hives, rashes, gastrointestinal problems and arthritis.
The goal is to create a euthyroidism condition which then stops the autoimmune response and the thyrotoxicosis. This is defined as the clinical remission.

Radioactive iodine (RAI) – it is often used as a more radical treatment if clinical remission cannot be obtained or sustained with ATDs. It may be used as a first line treatment for patients with a large goiter or opthalmopathy.
A single dose if often used, but the patient may need additional treatments. It is not used in young children, or pregnant or lactating mothers because of the potential risk of neoplasia.

Surgery – total or near total thyroidectomy is the most common surgery. RAI may be needed if hyperthyroidism continues after surgery. Surgery causes hypothyroidism and the need for lifelong replacement thyroid medication.

Learning Point
Only about 30% of children achieve clinical remission with ATD treatment, whereas 60-70% of adults achieve remission.
Longer term ATD may be necessary to achieve and keep children in clinical remission. If remission cannot be achieved or sustained, then other treatment is necessary.

Favorable predictors of Grave’s disease remission are older age group, presence of other autoimmune conditions and duration of ATD treatment more than 2 years.
Unfavorable predictors are younger age, large goiter, non-Caucasian race, biochemical severity and ATD medication non-compliance.

Questions for Further Discussion
1. How is Hashimoto’s thyroiditis different from Grave’s Disease?
2. What causes thyrotoxicosis?

http://pediatriceducation.org/2015/01/26/what-is-the-remission-rate-for-antithyroid-drug-treatment-for-hyperthyroidism-in-children/feed/0pediatriceducationminWhat Are Considerations for a Dancer to Begin Pointe Training?http://pediatriceducation.org/2015/01/19/what-are-considerations-for-a-dancer-to-begin-pointe-training/
http://pediatriceducation.org/2015/01/19/what-are-considerations-for-a-dancer-to-begin-pointe-training/#commentsMon, 19 Jan 2015 00:59:30 +0000http://pediatriceducation.org/?p=2608Continue reading →]]>Patient Presentation
During a discussion among several pediatricians about readiness for various sports training, one pediatrician asked what her colleagues did for young girls who wanted to start ballet dancing on pointe. There were a few general comments but nothing substantial except one person said that she thought there was a recent paper about the topic. Through a literature search, the pediatrician found a paper and then shared the information with her colleagues.

Discussion
Ballet dancing originated in Italy and was patronized by Queen Catherine de Médici of France who began the first ballet school in 1581. King Louis XIV of France was a major patron as he founded the Académie Royale de Danse in 1661. The Sun King was a performing dancer himself. The first documentation of a dancer performing en pointe (ie on pointe or on the tips of the toes) was in 1832 by Marie Talioni performing in La Sylphide.

Dancers are highly trained athletes and when dancing on pointe have the special appeal of appearing to effortlessly defy gravity. Ballet dancing shoes are slippers (made of soft leather, canvas, or satin, that has flexible, thin usually leather soles that that hug the foot), demi-pointe (similar to pointe shoes except for a smaller toe box and no shank in the arch, used more in Europe than United States) and pointe shoes. Pointe shoes have a toe box made of layers of paper, fabric and glue with a squared off end on the toe (i.e. the platform) that the dancer stands on and which provides the majority of the support. The shank is usually made of leather and supports the arch. Fabric (usually satin) surrounds these main pieces and the shoe is attached to the foot by elastic near the ankle and satin ribbons. A professional ballerina once described it to the author as “dancing in a Dixie® cup”. Pointe shoes are highly specialized equipment that needs a trained specialist to properly fit. The fit is extremely important for long-term injury prevention.

When dancing in ballet slippers, the relevé (elevated) foot position places the pressure on the metatarsals at 4x body weight. In demi-pointe or pointe shoes, the pressure is on the toes at 12 times body weight. The “ideal” foot is the “Giselle” foot where the first 3 toes are of relatively the same length allowing for distribution of the force across a greater area. Dancers with different anatomy still can be successful though. Dancing on pointe requires complete plantarflexion of the foot and ankle to 90° or more and is stabilized as the ankle “locks” into position with the subtalus locking between the tibia and calcaneus.

The change from dancing on the metatarsal heads to dancing on the toes seems like it should increase the likelihood of injuries but studies have not shown this. Specifically one study which looked at recreational (non-professional but serious) dancers before pointe shoes and after pointe shoe use did not find an increase in the likelihood of injuries during the past month or past 3 years. Longer term data was not evaluated. Also no studies have found that dancing on pointe before growth plate closure is linked to growth plate arrest, therefore radiographs are unnecessary to use as a factor for determining pointe readiness. Also the growth plates in these bones do not close until 18-20 years well after most dancers are already successfully dancing on pointe.

The quality of the preparatory training is paramount and experienced, ballet-specific instructors are important for preparation, decision making for placement into pointe shoes and training dancers using them. European ballets schools tend to be more rigorous with formalized systems of training and qualified instructors. This is not always true in the United States where dance studios may provide instruction in many different dance types and may not have instructors with specific training as ballet instructors. Studios can be placed under pressure to place dancers into pointe shoes because of the psychological aspirations of the dancer and family, and because of the financial pressures to do so.
As with any athletic activity, training and coaching under the direction of professional dancers with ballet-specific training is the most appropriate for dancers going on pointe.

Learning PointThere is no specific testing that can determine when a dancer can successfully transition to on pointe. One study found that 3 functional tests that help evaluate strength, flexability, alignment, postural control and balance correlated with teacher subjective rating for on pointe dancing readiness. These 3 are:

Airplane test – The dancer stands on one leg. The trunk is bent forward while the non-weight bearing leg is elevated behind them. The arms are extended in front creating the look of an airplane flying, or the letter “T” from the side or a Warrior III yoga pose.
The arms are lowered toward the ground, and the weight bearing leg is bent or folded in a controlled manner (i.e. plié) (<a href="View images here)

Sauté test – The dancer stands in a neutral pelvis, upright stable trunk position with arms at the side. The knees are bent and the dancer does a short jump into the air landing with control and a appropriate bending on the knees to absorb the shock. (<a href="View video here)

Topple test – a pirouette or turn is performed on one leg. The non-weight bearing leg’s hip is abducted and flexed with the foot aligned next to the weight being leg’s knee. The dancer should be able to do this in the relevé (elevated) foot position.(<a href="View video here“)

The great ballet choreographer George Balanchine once said that it took 4 or more years of serious training before a dancer was ready and with serious training starting around 7-8 years, this would be around 11-12 years or more.

A 2009 study ended with these considerations for pointe readiness. “A dancer should have adequate mental maturity and physical capability to begin dancing on pointe, rather than requiring a specific age or number of years. The dancer should have adequate flexibility in the foot and ankle complex to achieve full pointe, sufficient training to achieve proper placement, strength to achieve postural control and balance, proprioception, alignment, technique, mastery of movement, the ability to learn and perform choreography, and the ability to listen to apply corrections.” These ideas seem appropriate for any athlete including dancers.

Questions for Further Discussion
1. What resources do you have available locally to evaluate dancers for on pointe readiness?
2. What history questions should be gathered to evaluate dancers for on pointe readiness?

http://pediatriceducation.org/2015/01/19/what-are-considerations-for-a-dancer-to-begin-pointe-training/feed/0pediatriceducationminWhat Causes Muscle Cramps?http://pediatriceducation.org/2015/01/12/what-causes-muscle-cramps/
http://pediatriceducation.org/2015/01/12/what-causes-muscle-cramps/#commentsMon, 12 Jan 2015 00:58:18 +0000http://pediatriceducation.org/?p=2606Continue reading →]]>Patient Presentation A 10-year-old female came to clinic for her health maintenance examination. Her mother reported that she had night leg pain about 2-3 times per year over the past couple of years, but she had had one episode during the week before. The daughter would cry out and her mother would get there within 1-2 minutes. The girl would just say that her legs hurt and wanted them rubbed after which she would sleep without re-awakening. Once the mother was able to come to the bedside sooner and she was having unilateral muscle cramping. Again the mother massaged her leg and the daughter went back to sleep. She had no other sleep problems and had no problems during the day. Her mother said she didn’t seem to be restless when sleeping when she checked on her at night. She was a dancer but they were not aware of any increase in activity or changes in dietary intake on the days the episodes occurred. She and her mother denied that she sat or slept in abnormal positions. She had a good general diet and seemed to drink an appropriate amount of fluid. The past medical history showed a healthy female with some xerosis. The family history was negative for any neurological problems, sleep disorders, or leg cramping or pain. The review of systems was otherwise negative.

The pertinent physical exam showed a healthy female with normal vital signs. Her growth parameters showed a weight and height of 10-25% with normal velocities. HEENT was normal including her thyroid. Pubertal development was Tanner stage 1. Musculoskeletal examination was normal including muscle bulk. Palpation of the muscles did not produce any pain. Chvostek’s sign was negative and a Trousseau’s sign was not attempted.

The diagnosis of intermittent nocturnal leg pain possibly due to muscle cramping was made. The pediatrician discussed with the family that most leg pain and muscle cramps are idiopathic. Her history and physical examination did not reveal any other obvious causes of leg pain or muscle cramps and so the pediatrician recommended to monitor her. He recommended continuing to make sure she ate a healthy diet with calcium, potassium and magnesium foods and to drink an appropriate amount of fluid. He showed them some gentle stretching exercises that she could do before bed and told her to untuck the bedding to prevent the legs from having undue pressure put on them. They were to also keep a diary of the episodes and to call after the next one to discuss it.

Discussion
Leg pain is a relatively common problem in children. Usually it is idiopathic in origin but can be the sign of organic pathology. The differential diagnosis can be found here.

Noctural legs cramps have been found to occur in about 7% of healthy children. They start after age 8 and peak at 16-18 years of age. Cramps that are idiopathic are unilateral, and those with organic causes can be uni- or bi-lateral. Most episodes last only a few minutes but those lasting longer than 10 minutes are more likely to have an organic etiology.

Learning Point
The differential diagnosis of nocturnal muscle cramping in children includes:

Idiopathic – most common

Endocrine

Diabetes

Hypothyroidism

Hyperthyroidism

Exercise

Myalgia due to overuse

Compartment syndrome

Myoglobinuria

Fluids and Electrolytes

Poor fluid intake

Hypocalcemia

Hypokalemia

Hypomagnesemia

Metabolic alkalosis

Neurological

Contracture

Neuropathy

Sleep disorders

Restless legs syndrome – causes brief sustained muscle contractions

Periodic limb movement disorder

Other

Growing pains

Medication

Positioning, abnormal

Pregnancy

Vascular disease

Growing pains are a common problem but do not have hard muscular contraction. Growing pains are chronic pain of both legs that occur in the evening and night with normal physical examination and laboratory testing.
The pain is in the thigh or calf muscles. The pain can occur over weeks or months.

Questions for Further Discussion
1. What are indications for a sleep study for possible sleep disorders?
2. What laboratory testing could be done for muscle cramps and why?

http://pediatriceducation.org/2015/01/12/what-causes-muscle-cramps/feed/0pediatriceducationminIs A Specific Corticosteroid Better for Treatment of Asthma Than Another?http://pediatriceducation.org/2015/01/05/is-a-specific-corticosteroid-better-for-treatment-of-asthma-than-another/
http://pediatriceducation.org/2015/01/05/is-a-specific-corticosteroid-better-for-treatment-of-asthma-than-another/#commentsMon, 05 Jan 2015 00:21:20 +0000http://pediatriceducation.org/?p=2593Continue reading →]]>Patient Presentation An 11-year-old known-asthmatic male came to clinic for his health supervision visit. He was doing well in school, but his mother was concerned because he seemed to need his albuterol inhaler more and was coughing more at night. During the fall he had been playing soccer and although he took his inhaler before practices and games, he seemed to need the inhaler again during practices and games most days. Usually he also had no problems at night but his coughing was now waking the mother up at night at least 2-3 times per week. She had started giving him his inhaler before school on some days also. None of the symptoms improved as the fall frosts occurred. He said he had problems keeping up with the kids on the playground and had several episodes where his chest got tight at school.

The past medical history showed seasonal allergic rhinitis that was usually well controlled with cetirizine. He had never been hospitalized for asthma, and took oral steroids ~ 2 times a year for acute exacerbations. The family history was positive for asthma and allergies in multiple family members. The pertinent physical exam showed a healthy appearing male with normal vital signs and growth parameters. HEENT showed slightly pale mucous membranes and allergic shiners. Lungs were clear but after exercise in the room, he had some mild end expiratory wheezing. The rest of his examination was normal.

The diagnosis of uncontrolled asthma was made. An office peak flow meter reading was diminished from previous results. The resident seeing the child knew that he should probably start on an inhaled corticosteroid for better management, but he asked if one steroid was better than another. The staff pediatrician said that she didn’t think so because professional guidelines offered many different options plus the local pulmonologist seemed to use 2-3 different ones usually. “I’ll have to look at the guidelines again but I think if we use what the pulmonologist uses, he should get better,” she said. At follow-up in 4 weeks, the mother said that he was not coughing at night and he was using less albuterol although she could not quantify it. The physician did re-teaching about how to use the spacer and inhaler properly and had the mother start a symptom diary. The mother would contact the office with the amount of albuterol use over the next two weeks.

DiscussionAsthma is a chronic obstructive lung disease that affects many children and adults. There is a wide range of symptoms that people experience from occurring relatively rarely (ie intermittent asthma) to patients having daily symptoms of such intensity that they are life-threatening (ie chronic severe asthma). The goals of asthma management include patient education and medication management so patients have no or minimal symptoms, prevent exacerbations, have no activity restrictions, have normal pulmonary function tests, have no or minimal medication side effects and meet patient and family expectations. Well controlled asthma should have:

Asthma symptoms twice a week or less

Rescue bronchodilator use twice a week or less

No nighttime or early morning awakening

Daily, school and work activities should not be limited

Patient, family and physician believe asthma is well-controlled.

Normal pulmonary function tests

Assessment of asthma should occur routinely and especially if the patient’s symptoms are not well controlled.
This includes:

A step-wise approach for asthma has been advocated, where patients who are not well-controlled at a particular step, are given medication at the next higher step (ie “stepped-up”) until they are controlled.
Likewise, patients who are well-controlled may be candidates to “step-down” to a lower step in order to minimize the potential medication side effects.

The total ICS systemic concentration equals the total amount delivered to the lungs, plus the oral amount that is not deactivated by the liver. Overall, about 10-50% of the ICS is delivered to the lungs. Almost 100% of the ICS dose in the lung is bioavailable and will enter the circulation. Without a spacer or valved holding chamber, about 50-80% of the ICS medication is swallowed. Much of this will be deactivated by the liver, but some will enter the circulation. The overall oral ICS bioavailability (of the swallowed portion of the dose) has been reported as:

Flunisolide = 21%

Beclomethasone dipropionate = 20%

Triamcinolone acetonide = 10.6%

Budesonide = 11%

Fluticasone propionate = 1%

Mometasone = <1%

Questions for Further Discussion
1. How does asthma itself and treatments potentially affect children’s growth?
2. What are other potential side effects of pharmacological treatment of asthma?

http://pediatriceducation.org/2015/01/05/is-a-specific-corticosteroid-better-for-treatment-of-asthma-than-another/feed/0pediatriceducationminWhat Are Risk Factors for Progression To Severe Disease with Bronchiolitis?http://pediatriceducation.org/2014/12/15/what-are-risk-factors-for-progression-to-severe-disease-with-bronchiolitis/
http://pediatriceducation.org/2014/12/15/what-are-risk-factors-for-progression-to-severe-disease-with-bronchiolitis/#commentsMon, 15 Dec 2014 00:19:51 +0000http://pediatriceducation.org/?p=2591Continue reading →]]>Patient Presentation A 14-month-old male came to clinic during the winter with a 2 day history of low grade fever to 100.6°F and rhinitis. The evening before he began to have more coughing that was not episodic nor barky and his parent noticed that he seemed to be breathing fast. He was drinking about half of his normal amounts and was still urinating. His parent denied cyanosis. The past medical history showed a healthy male who was fully immunized. He had never wheezed in the past nor had atopic dermatitis. The family history was positive for his mother who had asthma. The review of systems was otherwise normal.

The pertinent physical exam showed a mildly ill appearing male with a respiratory rate of 35/minute, heart rate of 98 beats/minute and temperature of 99.4°. Pulse oximeter was 93%. His capillary refill was brisk and he had moderate secretions from his mouth and nose that were clear. HEENT was otherwise unremarkable. His lung examination had mild rhonchi that cleared with coughing. He also had some mild end-expiratory wheezing at both bases. He had no nasal flaring, intercostal retractions, abdominal breathing or trachael tugging.

The diagnosis of bronchiolitis was made. The pediatrician discussed the etiology and natural disease course with the family emphasizing that currently he was well-hydrated and was not having any increased work of breathing. She educated the parents on signs to call the clinic for and also had the nursing staff show the parents how to use nasal saline and suctioning at home. She also discussed other symptomatic treatment which could make the patient more comfortable such as antipyretics and/or humidified air.

DiscussionBronchiolitis is a clinical disease with following features: begins usually with rhinitis and cough that may progress to also having tachypnea, rales, wheezing and increased work of breathing shown by nasal flaring and/or accessory muscle use. The increased work of breathing may cause problems with feeding and hydration and also with mental status changes. It is usually seen in infants and children < 2 years of age. It is also usually seasonal (winter in upper North America) with 60-70% of cases being caused by respiratory syncytial virus but also human rhinorvirus, human metapneumovirus, influenza, adenovirus, coronavirus and human and parainfluenza viruses. Co-infections also are relatively common.

Diagnosis is clinical. Treatment includes secretion removal from the nose, oxygen therapy if needed, maintenance of hydration and monitoring.

Specifically, new guidelines from the American Academy of Pediatrics for infants < 23 months of age, also in accordance with the National Health Service in the United Kingdom (with minor variations), state that the following should or should not occur:

Yes/Should

Diagnose bronchiolitis clinically

Assess risk factors for severe disease

Assess exposure to tobacco smoke and encourage smoking cessation in family members

May consider administration of

Hypertonic saline in hospitalized infants

Oxygen if saturations are < 90%

Should administer

Fluids by nasogastric tube or intravenously for hydration if needed

Palivizumab prophylaxis for premature infants < 29 weeks and for infants with chronic lung disease or hemodynamically significant heart disease who require supplemental oxygen for at least the first 28 days of life.

Patient Care
1. When interacting with patients and their families, the health care professional communicates effectively and demonstrates caring and respectful behaviors.
2. Essential and accurate information about the patients’ is gathered.
3. Informed decisions about diagnostic and therapeutic interventions based on patient information and preferences, up-to-date scientific evidence, and clinical judgment is made.
4. Patient management plans are developed and carried out.
5. Patients and their families are counseled and educated.

Medical Knowledge
10. An investigatory and analytic thinking approach to the clinical situation is demonstrated.
11. Basic and clinically supportive sciences appropriate to their discipline are known and applied.

Practice Based Learning and Improvement
12. Evidence from scientific studies related to the patients’ health problems is located, appraised and assimilated.
13. Information about other populations of patients, especially the larger population from which this patient is drawn, is obtained and used.
14. Knowledge of study designs and statistical methods to appraisal clinical studies and other information on diagnostic and therapeutic effectiveness is applied.

Systems Based Practice
23. Differing types of medical practice and delivery systems including methods of controlling health care costs and allocating resources are known.
24. Cost-effective health care and resource allocation that does not compromise quality of care is practiced.